With these manipulations, the authors demonstrated that apoptosis is further potentiated during the postprandial period if the OB does not receive olfactory inputs, and is blocked by selective sleep deprivation after feeding. To balance this massive cell death, the authors also observed that local sensory deprivation promotes local recruitment of neuroblasts. They concluded that olfactory experience protects cells from death induced by postprandial sleep. Moreover, to disambiguate the role of food intake in this sensory input-dependent cell elimination, Trichostatin A the authors showed that apoptosis still increases in mice
entrained to the restricted food paradigm when no food is given but still
experience subsequent sleeping behavior. Therefore, a combination of olfactory experience and subsequent sleeping behavior mediates profound reorganization of OB networks within an hour after feeding. Adult-generated OB neurons are continually turned over, rather than simply added, and the precise balance between new and mature neurons is set through active elimination processes during a critical window. Previous studies have clearly demonstrated that odor learning in an associative task, but not simple exposure to an odor, can efficiently promote newborn cell survival within a critical period (14 to 35 days) after cell birth, while immature (7- Non-specific serine/threonine protein kinase to 13-day-old) and older cells are not affected (Mouret et al., 2008). Yokoyama and colleagues (2011) now describe a similar critical window for newborn neuron apoptosis in the context of postprandial selleck inhibitor sleep. This critical period corresponds to a maturation state when newborn cells first receive direct sensory inputs from principal cells of the OB and also top-down inputs from cortical regions such as olfactory cortex. These similar observations may encourage further
studies to establish whether olfactory learning-induced cell survival is related to the postprandial cell elimination reported by Yokoyama et al. (2011). Bearing in mind the relationship between sleep and learning (Maquet, 2001), finding a correlation between the two phenomena should not come as a surprise. Interestingly, the comparison between both behavioral contexts highlights the fact that isolated sensory input alone has no effect. It is only when sensory experience is associated with learning or with postprandrial sleep, two processes that involve top-down inputs to the OB, that it can affect apoptosis. Thus, by detecting the coincidence of sensory and top-down inputs, newborn neurons are ideally positioned to support long-term of memory processes (Lazarini and Lledo, 2011). One recent work has addressed the question of the biological significance of apoptosis in adult OB circuits (Mouret et al., 2009).